The partial pressure of ambient (and hence alveolar and arterial) oxygen falls in a near-linear relationship to altitude.
Below 3000 m there are few important clinical effects. Commercial aircraft are pressurized to 2750 m and the resulting hypoxia causes breathlessness only in those with severe cardiorespiratory disease. The incidence of thromboembolism is, however, slightly greater than at sea level in sedentary travellers on long flights.
Above 3000-3500 m, hypoxia causes a spectrum of related clinical syndromes that affect visitors to high altitudes, principally climbers, trekkers, skiers and troops. These conditions, which often coexist, occur largely during the acclimatization process. This may last some weeks, but enables man to live (permanently if necessary) at altitudes up to about 5600 m. At greater heights, although man can survive for days or weeks, deterioration due to chronic hypoxia is inevitable. It has now been demonstrated on several occasions that ascent to the highest of the world’s summits is possible without the use of supplementary oxygen. At the summit of Everest the barometric pressure is 34 kPa (253 mmHg). This enables an acclimatized mountaineer to have an alveolar P02 of 4.0-4.7 kPa (30-35 mmHg)-near the physiological limits of man.
Acute mountain sickness (AMS)
This term is used to describe the malaise, nausea, headache and lassitude that are common above 3500 m. Following arrival at this altitude there is usually a latent interval of 6-36 hours before the onset of symptoms.
Treatment is rest, with analgesics being given if necessary; recovery is almost invariable.
Prophylactic treatment with the carbonic anhydrase inhibitor acetazolamide is of value in reducing the symptoms of AMS, since these are partly due to the development of alkalosis. Acclimatizing by ascending gradually is the best prophylaxis.
In a minority of cases, the more serious sequelae of high-altitude pulmonary oedema (HAPO) and highaltitude cerebral oedema (HACO) occur. High-altitude pulmonary oedema Predisposing factors include youth, rapidity of ascent, heavy exertion and the presence of mountain sickness. Breathlessness, with frothy blood-stained sputum indicates established HAPO. Unless treated rapidly this leads to cardiorespiratory failure, collapse and death. Milder forms of HAPO are common, presenting with breathlessness that is not severe; it is important to recognize them.
High-altitude cerebral oedema
Cerebral oedema is a poorly understood sequel of hypoxia. It is probably the result of the abrupt increase in cerebral blood flow that occurs even at modest altitudes of 3500-4000 m. Headache is usual, and is accompanied by varying disturbances of cerebral function; drowsiness, ataxia, nystagmus and papilloedema are common. Coma and death follow if the condition progresses.
Any but the milder forms of AMS require urgent treatment. Oxygen should be given if it is available, and descent to a lower altitude should take place as quickly as possible. Dexamethasone or betamethasone are effective treatments in HAPO or HACO. Diuretics are of little value.
Small ‘flame’ haemorrhages in the nerve fibre layer of the retina are common above 5000 m. They are usually symptomless unless they cover the macula, when there is painless loss of central vision. Recovery is usual.
Prolonged residence between 5600 and 7000 m leads to a syndrome of weight loss, anorexia and listlessness after several weeks. Above 7500 m deterioration develops more quickly, although it is possible to survive for a week or more at altitudes over 8000 m.
Chronic mountain sickness
This rare syndrome occurs in long-term residents of high altitudes after several decades. It has been described clearly only in the Andes, but may occur in Tibet and elsewhere in central Asia.
Polycythaemia, drowsiness, cyanosis, finger clubbing, congested cheeks and ear lobes, and right ventricular enlargement occur. The condition is gradually progressive. By way of contrast, coronary artery disease and hypertension are rare in the native populations of high altitudes.